Abstract
SummaryWe recently suggested that the occurrence of ascorbic acid (AsA) in the apoplast of bell pepper fruit may be part of the protection mechanism against blossom-end rot (BER). In the present study, we determined AsA concentrations, changes in pH, and the activities of ascorbate oxidase (AO) in the apoplast and symplast of pepper fruit, in relation to fruit development and the occurrence of BER. In healthy pepper fruit, the concentrations of AsA in the symplast and apoplast increased during fruit development, whereas the activity of AO decreased when measured at the pH typical of each developmental stage. The apoplastic pH decreased from 6.2 in young fruit to 4.8 in mature red fruit; while the symplastic pH did not change during fruit development. Following high-temperature treatment (35°C for 48 h in the dark), the concentration of apoplastic AsA, and the activity of galacturonic acid reductase (which participates in the AsA biosynthetic pathway), decreased, while there was an increase in apoplastic pH. The AsA content decreased in the apoplast of BER-affected fruit, and the pH was more alkaline (pH 6.9) than in healthy fruit (pH 6.0). In young fruit with BER, the apoplastic AO activity increased and the symplastic galacturonic acid reductase activity was inhibited. We suggest that a reduction in apoplastic AsA concentration, an increase in apoplastic AO activity, and changes in apoplastic pH in fruit prone to BER may be part of the mechanism which leads to the occurrence of BER symptoms. Whether or not there are causal relationships between these changes is not yet clear.
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